Feto-maternal microchimerism: Memories from pregnancy
Blanca Cómitre-MarianoMagdalena Martínez‐GarcíaBárbara García-GálvezMaría Paternina-DieManuel DescoSusanna CarmonaMaría Victoria Gómez‐Gaviro
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Abstract:
There is a bidirectional transplacental cell trafficking between mother and fetus during pregnancy in placental mammals. The presence and persistence of fetal cells in maternal tissues are known as fetal microchimerism (FMc). FMc has high multilineage potential with a great ability to differentiate and functionally integrate into maternal tissue. FMc has been found in various maternal tissues in animal models and humans. Its permanence in the maternal body up to decades after delivery suggests it might play an essential role in maternal pathophysiology. Studying the presence, localization, and characteristics of FMc in maternal tissues is key to understanding its impact on the woman's body. Here we comprehensively review the existence of FMc in different species and organs and tissues, aiming to better characterize their possible role in human health and disease. We also highlight several methodological considerations that would optimize the detection, quantification, and functional determination of FMc.Keywords:
Microchimerism
Transplacental
Liposomes with different charge, size and lipid composition were injected i.v. into pregnant rats and rabbits and their uptake and transport across the placenta were studied. Results show that the placenta is very efficient in removing liposomes from the maternal circulation and that it takes up more liposomes per gram of tissue than the liver. Liposomes are degraded intracellularly in the placenta and the entrapped material is then transported across to the fetus as free molecules. Under the experimental conditions described in this article, no intact liposomes were found to be transported across the placenta. In comparison to the i.v. injection, infusion of liposomes into pregnant rabbits had greater effect on the localization of liposomal drug in the placenta and fetal blood. In summary, these results show that small unilamellar vesicles enhance delivery of drugs and nutrients to the placenta. They also suggest the possible danger of toxicity to the fetus if the expectant female is undergoing liposomal drug treatment.
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Fetal surgery is a promising strategy to treat fetuses with severe congenital abnormalities but its clinical applications are often limited by preterm labor. In normal pregnancy, multiple mechanisms protect the semi-allogeneic fetus from attack by maternal T cells. Maternal microchimerism (the presence of maternal cells in the fetus) has been suggested to be one mechanism of maternal-fetal tolerance in that it exposes the fetus to non-inherited maternal antigens and leads to the generation of fetal regulatory T cells that can suppress a maternal T cell response. Preterm labor may represent a breakdown of this robust tolerance network. We hypothesized that during inflammation-associated preterm labor, maternal leukocytes cross the maternal-fetal interface and enter the fetal circulation. Consistent with this hypothesis, we found that during preterm labor in mice, the percentage of maternal microchimerism in fetal blood increased and the frequency of fetuses with high levels of trafficking (greater than 0.5%) also increased. Finally, we showed that the maternal leukocytes trafficking into the fetus are primarily Gr-1+ cells in both syngeneic and allogeneic pregnancy, while T cell trafficking into the fetus specifically increases during allogeneic pregnancies. Our results demonstrate that trafficking of maternal leukocytes during pregnancy is altered during preterm labor. Such alterations may be clinically significant in affecting maternal-fetal tolerance.
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<i>In situ </i>placental perfusion has been used to study the role of the sheep placenta in fetal citrate metabolism. The perfusate citrate concentrations rose steadily to values higher than in fetal plasma. This rise was not influenced by intravenous administration of citrate to the ewe. Concentration and electropotential gradients indicate that transplacental passage is unlikely and the rise is probably due to placental synthesis. However, the quantity of citrate supplied to the fetus was calculated to be small compared with the fetal metabolic rate. Comparison with the guinea pig shows close similarity in fetal plasma concentrations and the amount of citrate formed per unit weight of fetus.
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The study of distribution of J125 labelled homologous alpha-fetoproteins (AFP) and heterologous antibodies (anti-AFP) in rats indicated some differences in the level of radioactivity of organs and tissues in animals, depending on age, especially in kidneys and large intestine. In normal pregnancy AFP passes through the placenta in both directions, but in rather less relative amounts from the fetus to mother. No labelled AFP was found in the amniotic fluid of fetuses 5 hours after its injection to pregnant mice. Anti-ATP injected in normal pregnant mice failed to pass through the placental barrier to the fetus, and radioactivity 5 hours following the injection was detected neither in fetal tissues nor in the amniotic fluid. After transplacental exposure of fetuses to methyl nitrosurea the labelled AFP was found in the amniotic fluid, while anti-AFP-both in fetal tissues and the amniotic fluid.
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The fetal side of hemochorial placentas from guinea pigs between 58 and 62 days gestation were perfused in situ. Concurrent measurements were made of the clearances of radiocalcium and tritiated water from maternal to fetal circulation of the placenta, transplacental potential difference (TPD), maternal plasma and perfusate Ca, Na, and K concentrations, maternal blood pressure, gross permeability of albumin in the placenta, and net water movements. Movement of Ca from dam to fetus appeared to occur against an electrochemical gradient and was not associated with the movements of Na and K across the placenta. A negative correlation between perfusate Na and K concentrations, not dependent on maternal plasma Na and K concentrations and abolished by high concentrations of Ca in the fetal circulation of the placenta, strongly supports the concept of a Na-K exchange mechanism in the placenta directed so that K is moved against a concentration gradient towards the dam. There was no evidence that the TPD existed at the site of maternal-fetal exchange for Ca, Na, or K.
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Effect of preparations from deer fetus and placenta on anti-aging of old male rats was studied. The results showed that the preparations from deer fetus and placenta inhibited MAO activities in brain and liver of rats significantly and decreased the contents of Lipofusin in heart and brain of rats. Deer fetus powder and deer fetus preparation Ⅱdecreased the MAO activities in brain by 67.74% and by 66.73% respectively, and the deer fetus preparation Ⅱdecreased the MAO activities in liver by 31.37%.It was concluded that the preparations from deer fetus and placenta have a good effect on anti-aging of old male rats, and the deer fetus preparation Ⅱ is more effective.
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The study of distribution of J125 labelled homologous alpha-fetoproteins (AFP) and heterologous antibodies (anti-AFP) in rats indicated some differences in the level of radioactivity of organs and tissues in animals, depending on age, especially in kidneys and large intestine. In normal pregnancy AFP passes through the placenta in both directions, but in rather less relative amounts from the fetus to mother. No labelled AFP was found in the amniotic fluid of fetuses 5 hours after its injection to pregnant mice. Anti-ATP injected in normal pregnant mice failed to pass through the placental barrier to the fetus, and radioactivity 5 hours following the injection was detected neither in fetal tissues nor in the amniotic fluid. After transplacental exposure of fetuses to methyl nitrosurea the labelled AFP was found in the amniotic fluid, while anti-AFP-both in fetal tissues and the amniotic fluid.
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The environment in which the fetus develops is critical for its survival and long-term health. The regulation of normal human fetal growth involves many multidirectional interactions between the mother, placenta, and fetus. The mother supplies nutrients and oxygen to the fetus via the placenta. The fetus influences the provision of maternal nutrients via the placental production of hormones that regulate maternal metabolism. The placenta is the site of exchange between mother and fetus and regulates fetal growth via the production and metabolism of growth-regulating hormones such as IGFs and glucocorticoids. Adequate trophoblast invasion in early pregnancy and increased uteroplacental blood flow ensure sufficient growth of the uterus, placenta, and fetus. The placenta may respond to fetal endocrine signals to increase transport of maternal nutrients by growth of the placenta, by activation of transport systems, and by production of placental hormones to influence maternal physiology and even behavior. There are consequences of poor fetal growth both in the short term and long term, in the form of increased mortality and morbidity. Endocrine regulation of fetal growth involves interactions between the mother, placenta, and fetus, and these effects may program long-term physiology.
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